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• Seventeen novel benzohydrazide derivatives of quinazoline-2,4(1 H ,3 H )-dione were synthesised using ultrasound-assisted, eco-friendly synthetic routes. • Compounds 7a and 7e showed very strong cytotoxicity against HCT-116, MCF-7, and PC3 cancer cell lines (EC₅₀ = 2.95–10.03 μM). • Compounds displayed selective cytotoxicity against cancer over normal WI38 cells. • Compounds showed Selective PARP-1 inhibition:7a: PARP-1 EC₅₀ = 0.068 μM vs PARP-2 EC₅₀ = 0.357 μM, 7e: PARP-1 EC₅₀ = 0.024 μM vs PARP-2 EC₅₀ = 0.119 μM. • Compound7a showed Lower PARP-1 DNA-trapping (EC₅₀ = 2.72 μM) than Olaparib, suggesting reduced toxicity risk. • Compounds7a and 7e bond to PARP-1 and PARP-2 in an inhibitory mode similar to Olaparib via π-π stacking and hydrogen bonds. • MD simulations confirm stable interactions with PARP-1, unstable with PARP-2. • Compounds showed Good oral bioavailability, no predicted hepatotoxicity, CNS toxicity, mutagenicity, or carcinogenicity in the in-silico studies they Lipinski’s & Veber’s drug-likeness rules. Poly(ADP-ribose) polymerase-1 (PARP-1) is a promising target for anticancer therapy. In this study, seventeen novel substituted quinazolin-2,4(1 H ,3 H )-dione derivatives were rationally designed, synthesized, and evaluated for their anti-proliferative activity against human cancer cell lines HCT-116, MCF-7, and PC3. Among these, compounds 7a and 7e exhibited the most potent cytotoxic effects, with EC₅₀ values ranging from 2.95 to 10.03 μM. They exhibited selective cytotoxicity towards tumor cell lines compared to normal cell lines, with EC 50 values of 87.92 ± 4.1 μM and 51.84 ± 2.9 μM, respectively, against WI38 cell lines. Mechanistic studies, including enzymatic assays, showed both compounds to be selective inhibitors of PARP-1 over PARP-2. where 7a and 7e showed PARP-1 inhibitory EC₅₀ values of 0.068 ± 0.0027 μM and 0.024 ± 0.0009 μM, respectively, compared to Olaparib (0.040 ± 0.002 μM) . For PARP-2, 7a and 7e exhibited EC₅₀ = 0.357 ± 0.014 μM and 0.119 ± 0.005 μM, respectively, confirming their selectivity. In DNA-trapping experiments, 7a and 7e demonstrated EC₅₀ = 2.720 μM and 0.890 μM, respectively. According to molecular docking studies, both compounds bind to PARP-2 less favorably and occupy the PARP-1 active site similarly to Olaparib, forming important π-π stacking and hydrogen-bonding interactions. In contrast to the unstable binding seen in the PARP-2 complex, molecular dynamics simulations conducted over a 50 ns period further confirmed that 7a binds selectively to PARP-1, exhibiting stable interactions and few conformational fluctuations. Favorable pharmacokinetic profiles, such as high oral bioavailability, drug-likeness, and the lack of anticipated hepatotoxicity, CNS liability, or carcinogenicity, were predicted by in silico ADMET analysis for 7a and 7e . When taken as a whole, these results show that 7a and 7e are promising lead compounds for the creation of selective PARP-1 inhibitors for cancer treatment.
Tawfik et al. (Wed,) studied this question.